Ventricular fibrillation [VF] is a cause of cardiac arrest and sudden cardiac death (SCD). During VF, the ventricular muscle contracts in a much less organized pattern than during normal sinus rhythm, so the ventricles fail to pump blood into the arteries and systemic circulation. VF is a sudden lethal arrhythmia responsible for many deaths in the Western world, mostly brought on by ischemic heart disease. VF which occurs in approximately 2 out of 10,000 people per year is a medical emergency. If the arrhythmia continues for more than a few seconds, blood circulation will cease, as evidenced by lack of pulse, blood pressure and respiration, and death will occur.
Despite much work, the underlying nature of VF is not completely understood. Most episodes of VF occur in diseased hearts, but others occur in structurally normal hearts. Much work still has to be done to elucidate the mechanisms of VF.
Ventricular tachycardia [VT] is a tachyarrhythmia originating from an ectopic ventricular region, characterized by a rate typically greater than 100 beats per minute and wide QRS complexes. VT may be monomorphic, i.e., originating from a single repeating pathway with identical QRS complexes, or polymorphic, i.e., following changing pathways, with varying QRS complexes. Non-sustained VT is defined as an episode of tachycardia of less than 30 seconds duration; longer runs are considered sustained VT.
No absolute ECG criteria exist for establishing the presence of VT. However, several factors suggest VT, including the following; Rate greater than 100 beats per minute (usually 150-200), wide QRS complexes (>120 ms), presence of atrioventricular (AV) dissociation, and fusion beats, which are integrated into the VT complex.
VT may develop without hemodynamic deterioration. Nevertheless, it often causes severe hemodynamic compromise and may deteriorate rapidly into VF. Therefore, this tachyarrhythmia also must be addressed swiftly to avoid morbidity or mortality.
VT is defined as three or more beats of ventricular origin in succession at a rate greater than 100 beats per minute. There are no normal-looking QRS complexes. The rhythm is usually regular, but on occasion it may be modestly irregular. The arrhythmia may be either well-tolerated or associated with grave, life-threatening hemodynamic compromise. The hemodynamic consequences of VT depend largely on the presence or absence or myocardial dysfunction (such as might result from ischemia or infarction) and on the rate of VT. Atrioventricular dissociation usually is present, which means that the sinus node is depolarizing the atria in a normal manner at a rate either equal to, or slower than, the ventricular rate. Thus, sinus P waves sometimes can be recognized between QRS complexes. They bear no fixed relation to the QRS complexes unless the atrial and ventricular rates happen to be equal. Conduction from atria to ventricles is usually prevented because the AV node or ventricular conduction system is refractory due to ventricular depolarizations caused by the VT.
VT is uncommon in the absence of apparent heart disease. It can develop as an early or a late complication of a myocardial infarction, or ischemia, during the course of cardiomyopathy, valvular heart disease, or myocarditis, or following heart surgery.
Myocardial infarcts heal by forming scar tissue which can lead to VT. This can occur days, months, or years after the infarction. VT can also result from anti-arrhythmic medications (an undesired effect) or from altered blood chemistries (such as low potassium or magnesium levels), pH (acid-base) changes, or insufficient oxygenation.
A common mechanism for VT is reentry (re-stimulation of the electrical conductive pathway from a single initial stimulus). “Torsade de pointes” is a form of VT with a specific variation or irregularity in the conduction of the ventricular stimulus.
In recent years, a preferred treatment for many chronic (long-term) VTs consists of implanting a cardiac device, such as an implantable cardioverter defibrillator (ICD). The ICD is usually implanted in the chest, like a pacemaker, and it is connected to the heart with intracardiac wires.
The ICD is programmed by the implanting physician to sense VT when it is occurring to administer a DC shock to convert/abort it. The ICD may also be programmed to pace the ventricles at a rapid rate, anti-tachycardia pacing (ATP), to attempt to entrain and halt the reentry circuit maintaining the VT. If the ATP is unsuccessful, an electrical shock is then given by the ICD for conversion. The VT may also require the use of concomitant anti-arrhythmic agents to prevent repeated firing of the ICD. Most VF episodes are preceded by VT, so it is highly desirable to prevent or halt VT before the arrhythmia degrades into VF where the heart is severely compromised hemodynamically.